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We selected 5 oncogenes with well-established roles in carcinogenesis -- CCND1, ErbB1, ErbB2, c-myc and ZNF217 -- to investigate the coexistence of their copy imbalances in relation to the clinico-pathological characteristics of ovarian tumors.Fluorescence in situ hybridization for the 5 genes was applied to a preexisting tissue microarray. 38 ovarian tumors were successfully analyzed for copy number changes of the 5 genes.At least one of these oncogenes was gained/amplified in 27 out of 38 tumors (71.1%). We report the highest frequency of c-myc genetic gain/amplification since it affected 42.1% of the ovarian tumors. We observed sequential involvement of copy number alterations of the other genes in the presence of c-myc disruption. The incidence of copy number changes of the 5 oncogenes -- both single and combinatorial -- was higher in high-grade tumors. All double aberrations in the serous group comprised c-myc and ZNF217copy number increases.Our results revealed a combination between copy number increases of c-myc and ZNF217, associated with serous histology. The data from this combined analysis of the 5 oncogenes could be used as a basis in considering the combined approach in molecular-based therapy of ovarian cancer.

Background: We selected 5 oncogenes with well-established roles in carcinogenesis – CCND1, ErbB1, ErbB2, c-mycand ZNF217– to investigate the coexistence of their copy imbalances in relation to the clinico-pathological characteristics of ovarian tumors. Materials and Methods: Fluorescence in situ hybridization for the 5 genes was applied to a preexisting tissue microarray. 38 ovarian tumors were successfully analyzed for copy number changes of the 5 genes. Results: At least one of these oncogenes was gained/amplified in 27 out of 38 tumors (71.1%). We report the highest frequency of c-mycgenetic gain/amplification since it affected 42.1% of the ovarian tumors. We observed sequential involvement of copy number alterations of the other genes in the presence of c-mycdisruption. The incidence of copy number changes of the 5 oncogenes – both single and combinatorial – was higher in high-grade tumors. All double aberrations in the serous group comprised c-mycand ZNF217copy number increases. Conclusions: Our results revealed a combination between copy number increases of c-mycand ZNF217, associated with serous histology. The data from this combined analysis of the 5 oncogenes could be used as a basis in considering the combined approach in molecular-based therapy of ovarian cancer.